Analgesic doses of morphine increase striatal dopamine turnover rate but this increase does not appear related to either an increase in the firing rate of dopaminergic neurons or to the stimulation of postsynaptic dopaminergic receptors. Opiate receptors are located on dopamine (DA) nerve terminals and in unknown sites of substantia nigra and hypothalamus pituitary system when these three sites appear to be involved in the regulation of DA function. We have established that stimulation of opioid receptors located on the terminals of DA neurons in striatum increases HVA accumulation. In contrast, stimulation of opiate receptors in SN result in a blockade of the haloperidol-induced activation of the nigrastriatal DA neurons. The prolactin secretin was used as a tool to investigate the action of opiates on hypothalamic DA neurons. Our results suggest that the opiate receptors located in the hypothalamus toxically control the prolactin release by a mechanism which is not directly related to the function of the DA system.